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首页> 外文期刊>Archives of Toxicology >Chemoprotective effects of captopril against cyclophosphamide-induced genotoxicity in mouse bone marrow cells.
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Chemoprotective effects of captopril against cyclophosphamide-induced genotoxicity in mouse bone marrow cells.

机译：卡托普利对小鼠骨髓细胞中环磷酰胺诱导的基因毒性的化学保护作用。

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摘要

The protective effects of captopril (CAP) against toxicity induced by cyclophosphamide (CP) in mice were investigated using the micronucleus assay for anticlastogenic activity in mouse bone marrow cells and liver glutathione (GSH) content. A single intraperitoneal (i.p.) injection of CAP at 50, 100, and 200 mg/kg 1 h prior to cyclophosphamide (50 mg/kg) reduced the frequency of micronucleated polychromatic erythrocytes (MnPCEs). All three doses of CAP significantly reduced the frequency of MnPCEs in mouse bone marrow compared to the group treated with CP alone (P<0.0001-0.01). CP significantly depleted the GSH content in liver but the application of CAP at a dose of 100 mg/kg 1 h before CP treatment repleted the GSH content. CAP exhibited concentration-dependent antioxidant activity, scavenging >96% of the 1,1-diphenyl-2-picryl hydrazyl free radicals when used at a concentration of 0.2 mM. It appears that CAP, due to its antioxidant activity and by increasing GSH levels, can modulate the reduced cellular thiol content induced by CP and reduce the genotoxicity of CP in bone marrow cells.
机译：使用微核试验检测小鼠骨髓细胞的抗成弹性活性和肝谷胱甘肽（GSH）含量，研究了卡托普利（CAP）对小鼠环磷酰胺（CP）诱导的毒性的保护作用。在环磷酰胺（50 mg / kg）之前1小时以50、100和200 mg / kg腹膜内（i.p.）CAP注射可降低微核多色红细胞（MnPCE）的频率。与单独使用CP治疗的组相比，所有三种剂量的CAP均显着降低了小鼠骨髓中MnPCE的频率（P <0.0001-0.01）。 CP显着消耗了肝脏中的GSH含量，但在CP治疗前1小时以100 mg / kg的剂量应用CAP可以补充GSH含量。 CAP表现出浓度依赖性的抗氧化剂活性，当以0.2 mM的浓度使用时，清除了> 96％的1,1-二苯基-2-吡啶基肼基自由基。似乎由于其抗氧化活性和通过增加谷胱甘肽水平，CAP可以调节由CP诱导的减少的细胞硫醇含量并降低CP在骨髓细胞中的遗传毒性。

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